1. Field of the Invention
The present invention relates generally to cardiac stimulating devices, such as pacemakers and defibrillators. More particularly, the present invention relates to a cardiac stimulating device that is capable of pacing all four chambers of the heart without requiring an epicardial lead. Still more particularly, the present invention relates to a pacer that includes pacing electrodes in each of the right atrium and right ventricle and in the coronary sinus/great cardiac vein for pacing the left atrium and left ventricle.
2. Description of the Related Art
In the normal human heart, illustrated in FIG. 1, the sinus (or sinoatrial (SA)) node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker by which rhythmic electrical excitation is developed. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers (or atria) at the right and left sides of the heart. In response to this excitation, the atria contract, pumping blood from those chambers into the respective ventricular chambers (or ventricles). The impulse is transmitted to the ventricles through the atrioventricular (AV) node, and via a conduction system comprising the bundle of His, or common bundle, the right and left bundle branches, and the Purkinje fibers. The transmitted impulse causes the ventricles to contract, the right ventricle pumping unoxygenated blood through the pulmonary artery to the lungs, and the left ventricle pumping oxygenated (arterial) blood through the aorta and the lesser arteries to the body. The right atrium receives the unoxygenated (venous) blood. The blood oxygenated by the lungs is carried via the pulmonary veins to the left atrium.
This action is repeated in a rhythmic cardiac cycle in which the atrial and ventricular chambers alternately contract and pump, then relax and fill. Four one-way valves, between the atrial and ventricular chambers in the right and left sides of the heart (the tricuspid valve and the mitral valve, respectively), and at the exits of the right and left ventricles (the pulmonic and aortic valves, respectively, not shown) prevent backflow or regurgitation of the blood as it moves through the heart and the circulatory system.
The sinus node is spontaneously rhythmic, and the cardiac rhythm originating from the primary natural pacemaker is termed sinus rhythm. This capacity to produce spontaneous cardiac impulses is called rhythmicity, or automaticity. Some other cardiac tissues possess this electrophysiologic property and hence constitute secondary natural pacemakers, but the sinus node is the primary natural pacemaker because it has the fastest spontaneous rate. The secondary natural pacemakers tend to be inhibited by the more rapid rate at which impulses are generated by the sinus node.
The resting rates at which sinus rhythm occurs in normal persons differ between age groups, generally ranging between 110 and 150 beats per minute ("bpm") at birth, and gradually slowing to the range between 65 and 85 bpm usually found in adults. The resting sinus rate (hereinafter termed simply the "sinus rate") varies from one person to another, and despite the aforementioned usual adult range, is generally considered to lie anywhere between 60 and 100 bpm (the "sinus rate range") for the adult population.
Disruption of the natural pacing system as a result of aging or disease is commonly treated by artificial cardiac pacing, by which rhythmic electrical discharges are applied to the heart at a desired rate from an implanted artificial pacemaker. An artificial pacemaker (or "pacer" as it is commonly labeled) is an implantable medical device which delivers electrical pulses to an electrode that is implanted adjacent or into the patient's heart in order to stimulate the heart so that it will beat at a desired rate. If the body's natural pacemaker performs correctly, blood is oxygenated in the lungs and efficiently pumped by the heart to the body's oxygen-demanding tissues. However, when the body's natural pacemaker malfunctions, an implantable pacemaker often is required to properly stimulate the heart. An in-depth explanation of certain cardiac physiology and pacemaker theory of operation is provided in U.S. Pat. No. 4,830,006.
Dilated cardiomyopathy is one type of malfunction of the heart. In dilated cardiomyopathy (DCM), the left, and sometimes also the right, ventricle balloons outward, increasing the diastolic (filled) volume from about 90 cc to about 260 cc. The ventricle wall is stretched thin and the force of contraction of the ventricle is greatly diminished. As a result, the ventricle empties inefficiently and incompletely. In addition, distortion of the ventricle causes distortion of the heart valves in turn, with the result that the valves do not close properly and pumping is less efficient. Because the left side of the heart does not pump effectively, backup of blood in the lungs occurs, causing pulmonary congestion and breathlessness. Additionally, if the right heart is affected, blood can back up in the legs, causing edema. In cases of severe DCM, death is either by pulmonary problems (infection secondary to congestion) or by sudden cardiac death (caused by ventricular fibrillation or electromechanical dissociation). DCM is divided into two main categories. Ischemic cardiomyopathy results when the heart muscle is deprived of oxygen, while when no obvious cause can be found it is called idiopathic cardiomyopathy. DCM is easily detectable using current diagnostic technology.
It is believed that pacing the left side of the heart, and in particular the left ventricle can improve circulation. More specifically, the left ventricle can be paced simultaneously with atrial pacing or shortly after a sensed atrial event, so that the ventricle contracts as blood flows into it from the left atrium. This accelerated ventricular pacing reduces regurgitation through the mitral valve, increases forward blood flow and helps prevent the left ventricle from overfilling.
Referring now to FIG. 2, which shows block diagram of a conventional dual-chamber pulse generator, a battery 11 supplies power for the pacer circuitry which is under the control of a microprocessor 12, which includes logic and memory. The atrial chamber is sensed with a sense amplifier 13 and paced with an output circuit 14. The ventricular chamber is sensed with a second sense amplifier 15 and paced with an output circuit 16. Bidirectional communication with an external programmer is accomplished with a telemetry circuit 17 and antenna. The lower rate behavior of the pacer is controlled by an accelerator 18, which measures exercise activity levels.
Referring now to FIG. 3, and by way of example only, two leads 20, 21 are shown connecting a conventional dual chamber pacemaker 22, such as that described in the preceding paragraph, to a heart. In a conventional dual chamber arrangement, leads 20, 21 are inserted in the right atrium and right ventricle, respectively. Each lead 20, 21 includes at least one stimulating electrode(s) for delivery of electrical impulses to excitable myocardial tissue in the appropriate chamber(s) inside the right side of the patient's heart. As shown in FIG. 3, each lead 20, 21 can include two electrodes, for example tip electrode 23 and ring electrode 24 on lead 20 and tip electrode 25 and ring electrode 26 on lead 21, to provide a total of four electrodes in the heart.
Two-, three-, and four-terminal devices all have been used or suggested as possible electrode schemes. Those skilled in the art will recognize that the pacing apparatus described herein is representative of a variety of devices. The present disclosure is provided merely to establish a context for the description of the invention below and is not intended to limit the scope of the invention in any way.
Pacers today are typically designed to operate in the "inhibited" mode. Inhibited mode pacemakers are also termed "demand" type pacemakers, because a pacing pulse is only generated when needed by the heart. Typically, demand pacemakers sense the patient's natural heart rate and apply stimuli only during periods when the heart rate falls below the desired pacing rate. In a demand pacer electrodes in the leads 20, 21 sense the occurrence of an intrinsic event and transmit this to the microprocessor 12 (FIG. 2) via the sense amplifiers 13 and 15. In addition, many pacers have the ability to sense metabolic demand and to modulate their pacing rate in response to sensed changes in metabolic demand. Pacemakers range from the simple fixed rate, single chamber device that provides demand pacing to highly complex models that provide fully automatic dual chamber pacing and sensing functions. The latter type of pacemaker is the latest in a progression toward physiologic pacing, that is, the mode of artificial pacing that most closely simulates natural pacing.
Because of the number of options available in pacer design, a convention has been established whereby specific pacer configurations are identified according to a code comprising three, four or five letters. The fifth code position describes the antitachycardia functions, if any. Because this position is not applicable to most commonly used pacemaker types, most common codes comprise either three or four letters. For this reason and for simplicity's sake, the fifth code position is omitted from the following table. Each code can be interpreted as follows:
______________________________________ Code position 1 4 ______________________________________ Function chamber chamber response to programmability, Identified paced sensed sensing rate modulation Options 0-none 0-none 0-none 0-none Available A-atrium A-atrium T- P-programmable V-ventricle V-ventricle triggered M-multi- D-dual I- programmable (A + V)) inhibited C-communicating R-rate modulating (T + 1) ______________________________________
For example, a DDD pacer paces and senses in both the ventricle and atrium and uses a dual type response. If atrial electrical activity is detected before the end of the atrial escape interval, atrial pacing is inhibited and a "sensed" atrio-ventricular (AV) delay is started. Otherwise, an atrial pacing pulse is issued and a "paced" AV delay is initiated. If ventricular electrical activity is sensed before the end of the AV delay, the ventricular pacing output is inhibited, otherwise a ventricular pacing pulse is delivered. Similarly, a WIR pacer paces and senses in the ventricle, uses an inhibited type response and is capable of modulating its rate activity in response to metabolic demand. Of the many possible pacer configurations, four or five are most commonly used. These are WI, WIR, DVI, DDD and DDDR.
Because access to the heart is usually made through the venous system, and more specifically through the superior vena cava, which empties into the right atrium, pacing leads are typically implanted in the right side of the heart. Access to the right ventricle is through the right atrium and tricuspid valve. In most cases, pacing of either the right atrium or the right ventricle will result in a corresponding stimulation of the left atrium or left ventricle respectively, after conduction delays that may not be physiologically and hemodynamically optimal. Thus, when it is desired to independently pace the left ventricle and/or atrium, as in the case of DCM, an alternative system is required.
Referring now to FIG. 4, pacing of the left atrium is often accomplished by providing bifurcating lead adapters 30 and 31, which each split a bipolar connection at the pacer header to form two unipolar leads. Alternatively, the pulse generator connector could be fitted with more receptacles which would accept the additional leads directly without the need for adapters such as 30, 31. This makes available third and fourth leads 35, 32. The third lead 35 is inserted through the ostium 36 of the coronary sinus 37 and positioned so that it is in contact with the wall of the coronary sinus adjacent the left atrium. Thus, three-chamber pacing/sensing can be achieved using three endocardial leads, leaving only the left ventricle un-paced.
Heretofore, independent pacing of the left ventricle has required placement of the fourth lead 32 as an epicardial lead, as there is no practical way to place an endocardial lead on the left side of the heart. Placement of a lead directly in the left ventricular chamber is associated with unacceptable risk of thromboembolism (blood clot) that could lodge in the brain, causing stroke, or in the arteries of the legs, which could lead to gangrene and amputation of the affected limb(s). Epicardial lead 32 contacts the outside, rather than the inside, of the heart, and therefore requires open chest surgery.
Because it is generally desirable to minimize the invasiveness of implantation procedures, there is a need for a pacing system for the left side of the heart that can be completely implanted intravenously and does not require open chest surgery.